Pub Date : 2026-01-17DOI: 10.1016/j.mehy.2026.111877
Bogdan-Alexandru Hagiu
The SARS-CoV-2 virus persists for up to 80 days in the brainstem of golden hamsters and this fact is correlated with dopaminergic dysfunctions and changes in the expression of some genes, including the suppression of DRD2. Since moderate-intensity physical exercise stimulates the expression of DRD2, it was hypothesized that this type of physical training can be used for the prophylaxis of neurological disorders in Long COVID. Testing the hypothesis can be performed on the same experimental animals and the results can be evidenced by histological and immunohistochemical analyses, transcriptomics, and behavioral tests. In this way, cases of Parkinson’s disease following SARS-C0V-2 infection could also be prevented, if this causal link is confirmed.
{"title":"Moderate-intensity exercise as a preventive strategy against dopaminergic dysfunction in Long COVID: A mechanistic hypothesis","authors":"Bogdan-Alexandru Hagiu","doi":"10.1016/j.mehy.2026.111877","DOIUrl":"10.1016/j.mehy.2026.111877","url":null,"abstract":"<div><div>The SARS-CoV-2 virus persists for up to 80 days in the brainstem of golden hamsters and this fact is correlated with dopaminergic dysfunctions and changes in the expression of some genes, including the suppression of DRD2. Since moderate-intensity physical exercise stimulates the expression of DRD2, it was hypothesized that this type of physical training can be used for the prophylaxis of neurological disorders in Long COVID. Testing the hypothesis can be performed on the same experimental animals and the results can be evidenced by histological and immunohistochemical analyses, transcriptomics, and behavioral tests. In this way, cases of Parkinson’s disease following SARS-C0V-2 infection could also be prevented, if this causal link is confirmed.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"208 ","pages":"Article 111877"},"PeriodicalIF":0.8,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-17DOI: 10.1016/j.mehy.2026.111876
Nikola Todorovic
Physical performance in hot environments is compromised by a combination of cardiovascular strain, thermoregulatory challenges, and oxidative, metabolic, and neuromuscular disruptions. While conventional pre-cooling strategies offer partial benefits, they often fail to prevent performance decline during prolonged exercise in the heat. Molecular hydrogen (H2), particularly in the form of hydrogen-rich water (HRW), has emerged as a promising modulator of redox homeostasis and cellular signaling in thermally stressed states. Recent evidence suggests that HRW ingestion may attenuate lactate accumulation and perceived exertion during endurance exercise, pointing to broader physiological roles beyond simple antioxidant action. I hypothesize that H2 acts as a context-sensitive ergogenic aid by modulating redox-sensitive signaling pathways, supporting mitochondrial bioenergetics, and influencing neuromuscular and afferent signaling, including mechanisms related to thermal discomfort and fatigue. Declines in breath hydrogen levels following exhaustive exercise further support the concept of hydrogen depletion as a marker or contributor to impaired performance and recovery, suggesting that hydrogen supplementation may be a potential solution to mitigate this occurrence. However, current studies remain limited in scope, often lacking methodological rigor and mechanistic depth. This article outlines a research framework for investigating H2 in heat-stressed exercise, highlighting key areas such as dose optimization, redox chronobiology, sex-specific responses, and longitudinal outcomes, with the aim of positioning H2 as a viable strategy for enhancing thermotolerance and performance.
{"title":"Molecular hydrogen and heat-stressed exercise: a mechanistic hypothesis and framework for future investigation","authors":"Nikola Todorovic","doi":"10.1016/j.mehy.2026.111876","DOIUrl":"10.1016/j.mehy.2026.111876","url":null,"abstract":"<div><div>Physical performance in hot environments is compromised by a combination of cardiovascular strain, thermoregulatory challenges, and oxidative, metabolic, and neuromuscular disruptions. While conventional pre-cooling strategies offer partial benefits, they often fail to prevent performance decline during prolonged exercise in the heat. Molecular hydrogen (H<sub>2</sub>), particularly in the form of hydrogen-rich water (HRW), has emerged as a promising modulator of redox homeostasis and cellular signaling in thermally stressed states. Recent evidence suggests that HRW ingestion may attenuate lactate accumulation and perceived exertion during endurance exercise, pointing to broader physiological roles beyond simple antioxidant action. I hypothesize that H<sub>2</sub> acts as a context-sensitive ergogenic aid by modulating redox-sensitive signaling pathways, supporting mitochondrial bioenergetics, and influencing neuromuscular and afferent signaling, including mechanisms related to thermal discomfort and fatigue. Declines in breath hydrogen levels following exhaustive exercise further support the concept of hydrogen depletion as a marker or contributor to impaired performance and recovery, suggesting that hydrogen supplementation may be a potential solution to mitigate this occurrence. However, current studies remain limited in scope, often lacking methodological rigor and mechanistic depth. This article outlines a research framework for investigating H<sub>2</sub> in heat-stressed exercise, highlighting key areas such as dose optimization, redox chronobiology, sex-specific responses, and longitudinal outcomes, with the aim of positioning H<sub>2</sub> as a viable strategy for enhancing thermotolerance and performance.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"208 ","pages":"Article 111876"},"PeriodicalIF":0.8,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-16DOI: 10.1016/j.mehy.2026.111886
Julio Buñay, Philippe de Medina, Marc Poirot, Sandrine Silvente-Poirot
Aging is characterized by a progressive decline in cellular stress responses, including oxidative stress resistance, mitochondrial quality control, DNA repair, and autophagy. Small extracellular vesicles (sEVs) released by all cell types are now recognized as key mediators of intercellular communication, particularly under stress conditions. sEVs derived from cells exposed to controlled, non-lethal stressors (e.g., hypoxia, oxidative, mitochondrial, or genotoxic stress) can carry protective molecules that promote stress adaptation and repair in recipient cells. We propose that stress-conditioned sEVs from young cells can restore adaptive stress responses and repair capacity in aging tissues by delivering molecular mediators that are diminished or dysregulated in aged cells. This concept builds on three well-established principles: (1) the content of sEVs reflects the physiological or stress state of the donor cell; (2) sEVs released from stressed cells convey adaptive mediators that promote resilience and repair in recipient cells; and (3) both stress-adaptive responses and intercellular communication are altered in the elderly. This hypothesis proposes that sEVs released by stress-conditioned young cells could constitute a novel gerotherapeutic approach capable of restoring adaptive stress responses and exerting beneficial effects on multiple hallmarks of aging in aged organisms. We discuss the biological rationale, supporting evidence, and experimental models to test this concept.
{"title":"Stress-conditioned small extracellular vesicles from young cells to restore resilience in aging","authors":"Julio Buñay, Philippe de Medina, Marc Poirot, Sandrine Silvente-Poirot","doi":"10.1016/j.mehy.2026.111886","DOIUrl":"10.1016/j.mehy.2026.111886","url":null,"abstract":"<div><div>Aging is characterized by a progressive decline in cellular stress responses, including oxidative stress resistance, mitochondrial quality control, DNA repair, and autophagy. Small extracellular vesicles (sEVs) released by all cell types are now recognized as key mediators of intercellular communication, particularly under stress conditions. sEVs derived from cells exposed to controlled, non-lethal stressors (e.g., hypoxia, oxidative, mitochondrial, or genotoxic stress) can carry protective molecules that promote stress adaptation and repair in recipient cells. We propose that stress-conditioned sEVs from young cells can restore adaptive stress responses and repair capacity in aging tissues by delivering molecular mediators that are diminished or dysregulated in aged cells. This concept builds on three well-established principles: (1) the content of sEVs reflects the physiological or stress state of the donor cell; (2) sEVs released from stressed cells convey adaptive mediators that promote resilience and repair in recipient cells; and (3) both stress-adaptive responses and intercellular communication are altered in the elderly. This hypothesis proposes that sEVs released by stress-conditioned young cells could constitute a novel gerotherapeutic approach capable of restoring adaptive stress responses and exerting beneficial effects on multiple hallmarks of aging in aged organisms. We discuss the biological rationale, supporting evidence, and experimental models to test this concept.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"208 ","pages":"Article 111886"},"PeriodicalIF":0.8,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-12DOI: 10.1016/j.mehy.2026.111878
Yuri Cordeiro Szeremeta
Perceived control is a transdiagnostic feature across chronic pain. The Locus of Control is a patient’s personality trait that refers to a belief about the extent to which they have control over their health outcomes. From a phenomenological point of view, the prevalence of internal or external dimensions of Locus of Control indicates how individuals operate certain cognitive systems and how they perceive different forces that influence their lives. Consequently, it is a key indicator of whether treatment will be successful or unsuccessful. However, the neural pathways and belief systems that underlie this personality trait remain poorly understood. This article raises the hypothesis that the theoretical basis of Active Inference may explain a propensity for external Locus of Control in chronic pain sufferers.
{"title":"Active Inference as a theoretical framework for external locus of control in chronic pain: the role of aberrant interoceptive integration","authors":"Yuri Cordeiro Szeremeta","doi":"10.1016/j.mehy.2026.111878","DOIUrl":"10.1016/j.mehy.2026.111878","url":null,"abstract":"<div><div>Perceived control is a transdiagnostic feature across chronic pain. The Locus of Control is a patient’s personality trait that refers to a belief about the extent to which they have control over their health outcomes. From a phenomenological point of view, the prevalence of internal or external dimensions of Locus of Control indicates how individuals operate certain cognitive systems and how they perceive different forces that influence their lives. Consequently, it is a key indicator of whether treatment will be successful or unsuccessful. However, the neural pathways and belief systems that underlie this personality trait remain poorly understood. This article raises the hypothesis that the theoretical basis of <em>Active Inference</em> may explain a propensity for external Locus of Control in chronic pain sufferers.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"208 ","pages":"Article 111878"},"PeriodicalIF":0.8,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145957763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-10DOI: 10.1016/j.mehy.2026.111875
Ariel A. Winnick , Tzu-Pu Chang
Patients with vestibular migraine (VM) are often prone to motion sickness, though the reason for this remains unclear. At the same time, migraine, and specifically VM, can be triggered by certain foods, but the underlying pathophysiology for this is also unknown. An earlier “toxin hypothesis” of motion sickness suggested that through evolution, the vestibular system developed as an alarm mechanism to detect ingested toxins, triggering the symptoms of motion sickness. Building on this idea, we revisit and extend it to an evolutionary hypothesis specifically linking VM and motion sickness. We propose that VM in migraineurs represents an overly sensitive alarm system capable of detecting even subtle neurotoxins in spoiled or degraded foods, substances commonly identified in modern society as migraine-triggers. This evolutionary hypothesis of VM provides a logical and contextual explanation for the observed links between VM, migraine-triggering foods, and motion sickness.
{"title":"Vestibular migraine, food triggers, and motion sickness: Revisiting an evolutionary hypothesis","authors":"Ariel A. Winnick , Tzu-Pu Chang","doi":"10.1016/j.mehy.2026.111875","DOIUrl":"10.1016/j.mehy.2026.111875","url":null,"abstract":"<div><div>Patients with vestibular migraine (VM) are often prone to motion sickness, though the reason for this remains unclear. At the same time, migraine, and specifically VM, can be triggered by certain foods, but the underlying pathophysiology for this is also unknown. An earlier “toxin hypothesis” of motion sickness suggested that through evolution, the vestibular system developed as an alarm mechanism to detect ingested toxins, triggering the symptoms of motion sickness. Building on this idea, we revisit and extend it to an evolutionary hypothesis specifically linking VM and motion sickness. We propose that VM in migraineurs represents an overly sensitive alarm system capable of detecting even subtle neurotoxins in spoiled or degraded foods, substances commonly identified in modern society as migraine-triggers. This evolutionary hypothesis of VM provides a logical and contextual explanation for the observed links between VM, migraine-triggering foods, and motion sickness.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111875"},"PeriodicalIF":0.8,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.mehy.2026.111874
Austin A. Barr
Opioid analgesics are indispensable for treating moderate-severe inpatient pain, yet even supervised use can precipitate long-term opioid use or opioid use disorder (OUD) in a small but consequential fraction of patients. Current prevention approaches emphasize screening, dosing, and duration, but rarely treat context as a modifiable risk factor. Pavlovian models show that drug effects become tightly linked to environmental cues, influencing tolerance, craving, and overdose risk; conversely, major contextual changes can disrupt addictive patterns. Virtual reality (VR) offers immersive, controllable contexts that already demonstrate analgesic and anxiolytic benefits, and can reliably engage drug-related cue learning. The present paper hypothesizes that systematically pairing inpatient opioid administration with distinctive, varied VR contexts could ‘capture’ opioid-associated learning within artificial contexts and reduce generalization of conditioned responses to post-discharge environments. Combined with VR’s intrinsic analgesic effects, which may reduce total opioid exposure, this strategy could act as a multi-level behavioral prophylaxis against persistent opioid use post-discharge. The conditioning rationale, potential risks, implementation principles, and a three-arm trial to test VR-based contextual prophylaxis during medical opioid therapy are discussed.
{"title":"Virtual reality-paired opioid analgesia as contextual prophylaxis against iatrogenic opioid addiction: a hypothesis","authors":"Austin A. Barr","doi":"10.1016/j.mehy.2026.111874","DOIUrl":"10.1016/j.mehy.2026.111874","url":null,"abstract":"<div><div>Opioid analgesics are indispensable for treating moderate-severe inpatient pain, yet even supervised use can precipitate long-term opioid use or opioid use disorder (OUD) in a small but consequential fraction of patients. Current prevention approaches emphasize screening, dosing, and duration, but rarely treat context as a modifiable risk factor. Pavlovian models show that drug effects become tightly linked to environmental cues, influencing tolerance, craving, and overdose risk; conversely, major contextual changes can disrupt addictive patterns. Virtual reality (VR) offers immersive, controllable contexts that already demonstrate analgesic and anxiolytic benefits, and can reliably engage drug-related cue learning. The present paper hypothesizes that systematically pairing inpatient opioid administration with distinctive, varied VR contexts could ‘capture’ opioid-associated learning within artificial contexts and reduce generalization of conditioned responses to post-discharge environments. Combined with VR’s intrinsic analgesic effects, which may reduce total opioid exposure, this strategy could act as a multi-level behavioral prophylaxis against persistent opioid use post-discharge. The conditioning rationale, potential risks, implementation principles, and a three-arm trial to test VR-based contextual prophylaxis during medical opioid therapy are discussed.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111874"},"PeriodicalIF":0.8,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.mehy.2026.111872
Lela Migirov
The human cochlea, the organ of hearing, is a conical spiral structure composed of the scala vestibuli, scala tympani, and scala media. Its spiral geometry is thought to arise from spatial constraints within the temporal bone and from the redistribution of wave energy, thereby enhancing sensitivity to lower-frequency, speech-related sounds. The cochlea is fully formed at birth, and congenital hearing loss is frequently associated with structural abnormalities of this organ. In this work, cochlear anatomy is described as a system of three non-intersecting spiral chambers that constitute a core architectural constraint governing sound propagation and encoding. It is hypothesized that the integrity of this non-intersecting spiral architecture is essential for normal auditory function, and that disruption of this organization contributes to congenital hearing impairment. Conceptual parallels between cochlear geometry, Fermat’s spiral, and spiral motifs in prehistoric art are presented as illustrative correspondences rather than causal relationships, based on their shared non-intersecting spiral pattern.
{"title":"A hypothesis on cochlear architecture: Non-intersecting spiral geometry as a determinant of auditory function","authors":"Lela Migirov","doi":"10.1016/j.mehy.2026.111872","DOIUrl":"10.1016/j.mehy.2026.111872","url":null,"abstract":"<div><div>The human cochlea, the organ of hearing, is a conical spiral structure composed of the scala vestibuli, scala tympani, and scala media. Its spiral geometry is thought to arise from spatial constraints within the temporal bone and from the redistribution of wave energy, thereby enhancing sensitivity to lower-frequency, speech-related sounds. The cochlea is fully formed at birth, and congenital hearing loss is frequently associated with structural abnormalities of this organ. In this work, cochlear anatomy is described as a system of three non-intersecting spiral chambers that constitute a core architectural constraint governing sound propagation and encoding. It is hypothesized that the integrity of this non-intersecting spiral architecture is essential for normal auditory function, and that disruption of this organization contributes to congenital hearing impairment. Conceptual parallels between cochlear geometry, Fermat’s spiral, and spiral motifs in prehistoric art are presented as illustrative correspondences rather than causal relationships, based on their shared non-intersecting spiral pattern.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111872"},"PeriodicalIF":0.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.mehy.2026.111873
Junhong Lü
The continuous emergence of SARS-CoV-2 variants challenges conventional antiviral strategies that targets highly mutable epitopes or enzymatic active sites. We propose a novel hypothesis centered on targeting the conserved dynamic regions of the SARS-CoV-2 spike (S) glycoprotein, which govern its large-scale conformational transitions. Through normal mode analysis (NMA), these regions have been identified as critical dynamic hotspots that facilitate an allosteric transition from the closed to the open, ACE2-accessible state. We hypothesize that small molecules or peptides designed to bind these hotspots could act as conformational locks, thereby providing broad-spectrum antiviral activity. The feasibility of targeting the physical dynamics of the spike protein is supported by independent studies on its mechanical vulnerability. While identifying druggable allosteric pockets and achieving experimental validation still need be overcome before practical realization, this strategy represents a paradigm shift from static, structure-based targeting to dynamic allostery. It offers a potentially variant-resilient therapeutic approach against both current and future threats from coronaviruses.
{"title":"Targeting conserved dynamic regions of SARS-CoV-2 spike protein identified by normal mode analysis for broad-spectrum antiviral therapy","authors":"Junhong Lü","doi":"10.1016/j.mehy.2026.111873","DOIUrl":"10.1016/j.mehy.2026.111873","url":null,"abstract":"<div><div>The continuous emergence of SARS-CoV-2 variants challenges conventional antiviral strategies that targets highly mutable epitopes or enzymatic active sites. We propose a novel hypothesis centered on targeting the conserved dynamic regions of the SARS-CoV-2 spike (S) glycoprotein, which govern its large-scale conformational transitions. Through normal mode analysis (NMA), these regions have been identified as critical dynamic hotspots that facilitate an allosteric transition from the closed to the open, ACE2-accessible state. We hypothesize that small molecules or peptides designed to bind these hotspots could act as conformational locks, thereby providing broad-spectrum antiviral activity. The feasibility of targeting the physical dynamics of the spike protein is supported by independent studies on its mechanical vulnerability. While identifying druggable allosteric pockets and achieving experimental validation still need be overcome before practical realization, this strategy represents a paradigm shift from static, structure-based targeting to dynamic allostery. It offers a potentially variant-resilient therapeutic approach against both current and future threats from coronaviruses.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111873"},"PeriodicalIF":0.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-30DOI: 10.1016/j.mehy.2025.111870
Paula A. Tello Prieto, David A. Miranda
We hypothesize that pain is the perception of a change in information by the organism that experiences it. This view departs from traditional biological, psychological, and social frameworks by framing pain not as a direct response to tissue injury or emotional distress, but as the detection of significant informational disturbance within the nervous system. We suggest that the nociceptive, pathological, and psychological forms of pain can be understood as variations in information flow rather than as distinct biological mechanisms. Information theory, particularly measures based on entropy, may offer a quantitative way to test this hypothesis by linking changes in neural information processing to subjective perception of pain. By proposing pain as an informational phenomenon, this hypothesis opens new perspectives for its diagnosis, management, and integration into a unified theoretical framework.
{"title":"Is pain perception of a change in information?","authors":"Paula A. Tello Prieto, David A. Miranda","doi":"10.1016/j.mehy.2025.111870","DOIUrl":"10.1016/j.mehy.2025.111870","url":null,"abstract":"<div><div>We hypothesize that pain is the perception of a change in information by the organism that experiences it. This view departs from traditional biological, psychological, and social frameworks by framing pain not as a direct response to tissue injury or emotional distress, but as the detection of significant informational disturbance within the nervous system. We suggest that the nociceptive, pathological, and psychological forms of pain can be understood as variations in information flow rather than as distinct biological mechanisms. Information theory, particularly measures based on entropy, may offer a quantitative way to test this hypothesis by linking changes in neural information processing to subjective perception of pain. By proposing pain as an informational phenomenon, this hypothesis opens new perspectives for its diagnosis, management, and integration into a unified theoretical framework.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111870"},"PeriodicalIF":0.8,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.mehy.2025.111871
Min Tae Kim
We propose a theoretical framework for engineering amoeboid cells as mobile bio-integrated ultrasonic emitters. The cells migrate within the interstitial space rather than within capillary lumens, where spatial constraints (5–8 m diameter) would otherwise prohibit transit. Amoebae in the 15–25 m size range can exploit their native locomotion mechanisms for environmental exploration, while transiently adopting an anchored state in which cytoskeletal tension stabilizes membrane resonance for efficient ultrasonic emission in the 0.5–2 MHz range. Acoustic radiation in this regime scales strongly with cell radius, enabling detectable remote signaling without requiring vascular circulation. The platform integrates genetically encoded piezoelectric or electromotile proteins (e.g., prestin variants), cytoskeletal tension tuning, and magnetoelastic nanoparticle resonators based on superparamagnetic iron oxide nanoparticles (SPIONs) to achieve controlled, directional ultrasound pulses under an external magnetic field. This dual-mode architecture — mobile sensing and anchored communication — supports distributed biological navigation, intercellular messaging, and potential therapeutic actuation. The framework establishes feasibility conditions and design parameters for future experimental realization.
{"title":"Bio-integrated ultrasound emission hypothesis in engineered amoeboid cells","authors":"Min Tae Kim","doi":"10.1016/j.mehy.2025.111871","DOIUrl":"10.1016/j.mehy.2025.111871","url":null,"abstract":"<div><div>We propose a theoretical framework for engineering amoeboid cells as mobile bio-integrated ultrasonic emitters. The cells migrate within the interstitial space rather than within capillary lumens, where spatial constraints (5–8 <span><math><mi>μ</mi></math></span>m diameter) would otherwise prohibit transit. Amoebae in the 15–25 <span><math><mi>μ</mi></math></span>m size range can exploit their native locomotion mechanisms for environmental exploration, while transiently adopting an anchored state in which cytoskeletal tension stabilizes membrane resonance for efficient ultrasonic emission in the 0.5–2 MHz range. Acoustic radiation in this regime scales strongly with cell radius, enabling detectable remote signaling without requiring vascular circulation. The platform integrates genetically encoded piezoelectric or electromotile proteins (e.g., prestin variants), cytoskeletal tension tuning, and magnetoelastic nanoparticle resonators based on superparamagnetic iron oxide nanoparticles (SPIONs) to achieve controlled, directional ultrasound pulses under an external magnetic field. This dual-mode architecture — mobile sensing and anchored communication — supports distributed biological navigation, intercellular messaging, and potential therapeutic actuation. The framework establishes feasibility conditions and design parameters for future experimental realization.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"207 ","pages":"Article 111871"},"PeriodicalIF":0.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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